Cancer-associated fibroblasts in colorectal cancer.

S Kamali Zonouzi, P S Pezeshki, S Razi, N Rezaei

Journal: Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico 2022;24(5):757-769

PMID: 34839457

Abstract

Colorectal cancer (CRC) is one of the leading causes of mortality among cancers. Many aspects of this cancer are under investigation to find established markers of diagnosis, prognosis, and also potential drug targets. In this review article, we are going to discuss the possible solution to all these aims by investigating the literature about cancer-associated fibroblasts (CAFs) involved in CRC. Moreover, we are going to review their interaction with the tumor microenvironment (TME) and vitamin D and their role in tumorigenesis and metastasis. Moreover, we are going to expand more on some markers produced by them or related to them including FAP, a-SMA, CXCL12, TGF- β, POSTN, and β1-Integrin. Some signaling pathways related to CAFs are as follows: FAK, AKT, activin A, and YAP/TAZ. Some genes related to the CAFs which are found to be possible therapeutic targets include COL3A1, JAM3, AEBP1 and, CAF-derived TGFB3, WNT2, and WNT54.

© 2021. The Author(s), under exclusive licence to Federación de Sociedades Españolas de Oncología (FESEO).

Address: School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Tehran, Iran.; School of Medicine, Iran University of Medical Sciences, Tehran, Iran.; Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Dr Qarib St, Keshavarz Blvd, 14194, Tehran, Iran. [email protected].; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. [email protected].; Cancer Immunology Project (CIP), Universal Scientific Education and Research Network (USERN), Stockholm, Sweden. [email protected].

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